200 BULLETIN OF THE BUREAU OF FISHERIES. 



inside the cell wall. These are probably artifacts. The older bacilli (fig. 9, pi. xx) taper 

 at one end. They were at first taken for protozoan spores. These bacilli occur by 

 thousands in and near degenerate epidermis and muscle tissue. It is not unusual to find 

 them grouped in the form of the cell which they have completely destroyed. They are 

 then of nearly uniform size (fig. 10, pi. xx); but between individuals of separate groups, 

 there is often a great difference in size. They stain, as a rule, with methylene blue, 

 gentian violet, toluidin blue, and Giemsa stain. Inside the host cells (fig. 6, pi. xx) and 

 when first set free from them they stain, if at all, with great difficulty. This may no 

 doubt be due to a zoogloeic condition. In smears, the stretching of this secretion causes 

 the bacilli to be drawn into long parallel rows. The secretion then resembles elastic 

 connective tissue fibers and the bacteria replace the connective tissue nuclei. At times 

 the zoogloea is not noticeable. (Fig. 8 and 10.) 



To what extent toxins emanating from the short bacillus are the cause of the death 

 and disintegration of the host tissues we can judge from the following facts : As already 

 stated, this bacillus is not to be found throughout large areas of atrophied muscle and 

 integument. If the toxin emanating by diff'usion from a localized organism brought 

 about the decadence of a tissue, one Would expect the evidences of such decadence 

 to indicate a uniform advance of said toxin in the same direction through a given tissue; 

 but, as we have seen, the atrophy of muscle fibers is limited to a certain few in a large 

 number of normal cells, or there may even be a few normal fibers extending through and 

 far into a necrotic region. The same relations prevail more or less in the epidermis. 

 If the short bacillus is to be regarded as a saprophyte, then some more virulent primary 

 organism must be present. In the diseased gills the abundance of AI. musculi and the 

 extent of injury in its immediate presence point to the sporozoon as the primary agent. 

 There are a few places in the gill tissue where the short bacillus is abundant, but, as 

 would be expected of a saprophyte, in very degenerate tissue only. Such seems to be 

 its relation to all the tissues. 



There are also tissues in which nothing but the long bacillus can be recognized as 

 the agent of primary degeneration. While never abundant, it may be observed more 

 frequently than the short bacillus in fresh smears of infected tissue. After about 24 hours 

 the latter appear in clusters in the muscle fibers occupying excavations of regular ovoid 

 contour. The long type occurs less frequently in tissues that are completely atrophied 

 than in those which just begin to show signs of decadence. Fresh muscle, in the latter 

 condition, may have the long bacilli more or less abundantly distributed under the 

 sarcolerama, but never in compact groups, a condition which is characteristic of the 

 short form. In sections, the long type has been encountered, one or two at a time, 

 in muscle fibers at or near the region of advancing degeneration, and occupying irregular 

 transverse clefts in the scarcoplasm (similar to those in fig. 4, pi. xx). But these cavities 

 seem to be much too large to be considered the excavations of so few of these minute 

 organisms. Their toxins may precede them and the transverse cleavage of the muscle 

 fiber may be due to subsequent mechanical forces. On the other hand, the bacillus is 

 quite as likely to creep into the crevices in the sarcoplasm as are the blood tissues 

 (p. 198). Its presence is therefore not necessarily evidence that it is the cause of the 

 crevices. In one stained smear, some of the muscle fibers of which are completely 

 hypertrophied, the long bacillus is very abundant, especially in the connective tissue. 

 There is no evidence of the admixture of fluid from purulent tissue such as is frequently 



